Glucose signal in the nucleus of the vagus nerve modulates the cyclicity of gastric motility in rats

Takeo, Satoshi; Sandoh, Norimasa; Aono, Takashi

doi:10.1016/0006-8993(94)91832-5

Cited by 10 publications

(15 citation statements)

References 12 publications

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“…A central site of action of glucose in the modulation of gastrointestinal functions still appears to arouse controversy. Several studies have demonstrated profound alterations in gastric tone and motility in response to microinjection of glucose directly into the NTS or the DMV (24,58,61), whereas other studies did not observe any noticeable effect following intracisternal application of glucose (79). It is unlikely that these differences can be explained entirely through the disparities in experimental techniques although the latter study used relatively modest alterations in central glucose levels.…”

Section: Discussionmentioning

confidence: 90%

“…At the central level, microinjection of glucose into either the DMV or the NTS decreases gastric motility and secretion (24,58,61) although a recent study did not observe any effects on gastric relaxation following mild hyperglycemia due to intracisternal application of dextrose (79). Several studies have demonstrated that subpopulations of NTS and DMV neurons respond to alterations in glucose by either increasing or decreasing their activity (1,6,7,18,19,48,73,77,78), and we have demonstrated recently that synaptic transmission from the central nerve terminals of vagal afferent neurons is dependent upon glucose concentration (73), suggesting that the synaptic connections between vagal afferent fibers and NTS neurons are a probable site of action of glucose to modulate vagovagal reflexes.…”

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confidence: 99%

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Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors

Wan

Browning²

2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Acute hyperglycemia has profound effects on vagally mediated gastrointestinal functions. We have reported recently that the release of glutamate from the central terminals of vagal afferent neurons is correlated directly with the extracellular glucose concentration. The present study was designed to test the hypothesis that 5-HT(3) receptors present on vagal afferent nerve terminals are involved in this glucose-dependent modulation of glutamatergic synaptic transmission. Whole-cell patch-clamp recordings were made from neurons of the nucleus tractus solitarius (NTS) in thin rat brainstem slices. Spontaneous and evoked glutamate release was decreased in a concentration-dependent manner by the 5-HT(3) receptor selective antagonist, ondansetron. Alterations in the extracellular glucose concentration induced parallel shifts in the ondansetron-mediated inhibition of glutamate release. The changes in excitatory synaptic transmission induced by extracellular glucose concentration were mimicked by the serotonin uptake inhibitor, fenfluramine. These data suggest that glucose alters excitatory synaptic transmission within the rat brainstem via actions on tonically active 5-HT(3) receptors, and the number of 5-HT(3) receptors on vagal afferent nerve terminals is positively correlated with the extracellular glucose concentration. These data indicate that the 5-HT(3) receptors present on synaptic connections between vagal afferent nerve terminals and NTS neurons are a strong candidate for consideration as one of the sites where glucose acts to modulate vagovagal reflexes.

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Section: Discussionmentioning

confidence: 90%

mentioning

confidence: 99%

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors

Wan

Browning²

2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…injection of L‐dopa occurs in the AP, medial NTS besides the CeA and LPBe. The NTS, the major relay center of visceral afferents 59 is directly connected to the LPBe, PVN, and CeA, 60–62 and plays a role in the regulation of gastric motility, 63,64 which can be involved in the inhibition of gastric emptying by i.p. L‐dopa.…”

Section: Discussionmentioning

confidence: 99%

Ghrelin prevents levodopa‐induced inhibition of gastric emptying and increases circulating levodopa in fasted rats

Wang

Murphy

Stengel

et al. 2012

Neurogastroenterology Motil

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Background Levodopa (L-dopa) is the most commonly used treatment for alleviating symptoms of Parkinson's disease. However, L-dopa delays gastric emptying, which dampens its absorption. We investigated whether ghrelin prevents L-dopa action on gastric emptying and enhances circulating L-dopa in rats. Methods Gastric emptying of non-nutrient methylcellulose/phenol red viscous solution was determined in fasted rats treated with orogastric or intraperitoneal (ip) L-dopa, or intravenous (iv) ghrelin 10 min before orogastric L-dopa. Plasma L-dopa and dopamine levels were determined by high pressure liquid chromatography. Plasma acyl ghrelin levels were assessed by radioimmunoassay. Fos expression in the brain was immunostained after iv ghrelin (30 μg kg-1) 10 min before ip L-dopa. Key Results L-dopa (5 and 15 mg kg-1) decreased significantly gastric emptying by 32% and 62% respectively when administered orally, and by 91% and 83% when injected ip. Ghrelin (30 or 100 μg kg-1, iv) completely prevented L-dopa's (15 mg kg-1, orogastrically) inhibitory action on gastric emptying and enhanced plasma L-dopa and dopamine levels compared with vehicle 15 min after orogastric L-dopa. L-dopa (5 mg kg-1) did not modify plasma acyl ghrelin levels at 30 min, 1 and 2 h after iv injection. L-dopa (15 mg kg-1, ip) induced Fos in brain autonomic centers, which was not modified by iv ghrelin. Conclusions & Inferences Ghrelin counteracts L-dopa-induced delayed gastric emptying but not Fos induction in the brain and enhances circulating L-dopa levels. Potential therapeutic benefits of ghrelin agonists in Parkinson's disease patients treated with L-dopa remain to be investigated.

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“…i.e., the nucleus tractus solitarius (NTS), the dorsal motor nucleus of the vagus (DMV), and the area postrema] react promptly to changes in glucose levels (3,4,8,14,20,47,52). In vivo, these changes in the activity of DVC neurons in response to blood glucose are transmitted to the pancreas, via the vagus nerve, to modulate glucose homeostasis (5)(6)(7)26).…”

Section: Glucose-sensitive Neurons In the Dorsal Vagal Complex [Dvc;mentioning

confidence: 99%

“…These data indicate that 1) GLP-1 may act on DMV neurons to control pancreatic endocrine secretion, 2) the effects of GLP-1 on pancreasprojecting DMV neurons are mediated both via a direct excitation of their membrane as well as via an effect on local circuits, and 3) the GLP-1-responsive neurons (i.e., putative endocrine secretioncontrolling neurons) could be distinguished from neurons responsive to PP (i.e., putative exocrine secretion-controlling neurons). brain stem; electrophysiology; vagus; pancreas GLUCOSE-SENSITIVE NEURONS in the dorsal vagal complex [DVC; i.e., the nucleus tractus solitarius (NTS), the dorsal motor nucleus of the vagus (DMV), and the area postrema] react promptly to changes in glucose levels (3,4,8,14,20,47,52). In vivo, these changes in the activity of DVC neurons in response to blood glucose are transmitted to the pancreas, via the vagus nerve, to modulate glucose homeostasis (5-7, 26).…”

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confidence: 99%

Glucagon-like peptide-1 excites pancreas-projecting preganglionic vagal motoneurons

Wan

Coleman

Travagli³

2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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Glucagon-like peptide-1 (GLP-1) increases pancreatic insulin secretion via a direct action on pancreatic beta-cells. A high density of GLP-1-containing neurons and receptors is also present in brain stem vagal circuits; therefore, the aims of the present study were to investigate 1) whether identified pancreas-projecting neurons of the dorsal motor nucleus of the vagus (DMV) respond to exogenously applied GLP-1, 2) the mechanism(s) of action of GLP-1, and 3) whether the GLP-1-responsive neurons (putative modulators of endocrine secretion) could be distinguished from DMV neurons responsive to peptides that modulate pancreatic exocrine secretion, specifically pancreatic polypeptide (PP). Whole cell recordings were made from identified pancreas-projecting DMV neurons. Perfusion with GLP-1 induced a concentration-dependent depolarization in approximately 50% of pancreas-projecting DMV neurons. The GLP-1 effects were mimicked by exendin-4 and antagonized by exendin-(9-39). In approximately 60% of the responsive neurons, the GLP-1-induced depolarization was reduced by tetrodotoxin (1 microM), suggesting both pre- and postsynaptic sites of action. Indeed, the GLP-1 effects were mediated by actions on potassium currents, GABA-induced currents, or both. Importantly, neurons excited by GLP-1 were unresponsive to PP and vice versa. These data indicate that 1) GLP-1 may act on DMV neurons to control pancreatic endocrine secretion, 2) the effects of GLP-1 on pancreas-projecting DMV neurons are mediated both via a direct excitation of their membrane as well as via an effect on local circuits, and 3) the GLP-1-responsive neurons (i.e., putative endocrine secretion-controlling neurons) could be distinguished from neurons responsive to PP (i.e., putative exocrine secretion-controlling neurons).

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Glucose signal in the nucleus of the vagus nerve modulates the cyclicity of gastric motility in rats

Cited by 10 publications

References 12 publications

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors

Ghrelin prevents levodopa‐induced inhibition of gastric emptying and increases circulating levodopa in fasted rats

Glucagon-like peptide-1 excites pancreas-projecting preganglionic vagal motoneurons

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Glucose signal in the nucleus of the vagus nerve modulates the cyclicity of gastric motility in rats

Cited by 10 publications

References 12 publications

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT3 receptors

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT3 receptors

Ghrelin prevents levodopa‐induced inhibition of gastric emptying and increases circulating levodopa in fasted rats

Glucagon-like peptide-1 excites pancreas-projecting preganglionic vagal motoneurons

Contact Info

Product

Resources

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Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors